A synthetic prostaglandin E1 analogue, misoprostol, ameliorates paclitaxel-induced oxidative damage in rat brain

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dc.authoridGUR, FATIH MEHMET/0000-0001-7748-3272
dc.contributor.authorGur, Fatih Mehmet
dc.contributor.authorBilgic, Sedat
dc.date.accessioned2024-11-07T13:31:46Z
dc.date.available2024-11-07T13:31:46Z
dc.date.issued2022
dc.departmentNiğde Ömer Halisdemir Üniversitesi
dc.description.abstractThe main objective of our study was to examine the protection of misoprostol (MP) on paclitaxel (PAX) side effects in rat brains. Twenty-eight female Sprague-Dawley rats were provided to form 4 groups, each containing seven rats: the control group was given 1 mL of 0.9% NaCl intraperitoneally (i.p.) and 1 mL of 0.9% NaCl orally for six days. In treatment groups, each rat was injected with 2 mg/kg PAX i.p. on days 0, 2, 4, and 6 of the study, and 0.2 mg/kg/day MP was given by oral gavage for six days. Levels of malondialdehyde (MDA) and glutathione (GSH), activities of superoxide dismutase (SOD), and catalase (CAT) of tissue samples were measured. In immunohistochemical analyzes, it was observed that tumor necrosis factor-alpha (TNF-alpha) and cleaved caspase-3 expression in the cerebellum hippocampus and cerebral cortex were increased in the PAX group compared to the other groups. The increase in TNF-alpha and cleaved caspase-3 expression detected in PAX group rats were significantly decreased in the PAX + MP group. The results obtained in this study confirm the hypotheses that PAX can increase apoptosis in brain tissue both directly and through cytokines such as TNF-alpha. It also shows that MP can be used as a protective and therapeutic pharmacological agent against the harmful effects of PAX on brain tissue. In addition, it seems that the use of MP can improve PAX-induced brain damage by preventing oxidative damage.
dc.identifier.doi10.1016/j.prostaglins.2022.106663
dc.identifier.issn1098-8823
dc.identifier.issn2212-196X
dc.identifier.pmid35809771
dc.identifier.scopus2-s2.0-85134316549
dc.identifier.scopusqualityQ2
dc.identifier.urihttps://doi.org/10.1016/j.prostaglins.2022.106663
dc.identifier.urihttps://hdl.handle.net/11480/15041
dc.identifier.volume162
dc.identifier.wosWOS:000830530700001
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherElsevier Science Inc
dc.relation.ispartofProstaglandins & Other Lipid Mediators
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_20241106
dc.subjectPaclitaxel
dc.subjectMisoprostol
dc.subjectCaspase-3
dc.subjectOxidative stress
dc.subjectBrain damage
dc.subjectTNF-
dc.titleA synthetic prostaglandin E1 analogue, misoprostol, ameliorates paclitaxel-induced oxidative damage in rat brain
dc.typeArticle

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